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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatitis B virus (HBV) is transmitted by parenteral, sexual and perinatal routes. While fulminant hepatitis may occur in 1% of cases of symptomatic acute hepatitis, the principal problem of HBV infection is that it may become chronic, classically defined by carriage of HB surface antigens (HBsAg) for more than 6 months. This occurs in only 0.5 to 3% of immunocompetent adults but more frequently in children (up to 90%) and in immune-compromised patients (30 to 100%). The course of chronic HBV infection is characterized by variations in viral replication with spontaneous reactivation or discontinuation, and potential exacerbations observed clinically or by laboratory testing. The pathogenesis of HBV infection is mainly immune-mediated, resulting from host-virus interactions but also from the complexity of the virus itself (integration, mutation, occult replication). These factors explain the variety of presentations of chronic HBV infection, which range from immune tolerance to inactive carriage of HBsAg, passing through a stage of immune clearance, where chronic active hepatitis which may lead to cirrhosis (yearly incidence of 1.3 to 5.9%). Cirrhosis may be complicated by portal hypertension, liver failure, or hepatocellular carcinoma, which together explain 80% of the morbidity and mortality associated with HBV. The 5-year survival rate for HBV-related cirrhosis ranges from 52 to 82%. Immunosuppression, hepatitis D virus superinfection, and chronic alcohol consumption are the principal factors that modify this natural history. Chronic HBV infection is a major public health problem, particularly in developing countries, and it requires that efforts to make HBV vaccination universal be intensified.
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PMID:[Natural history of hepatitis B infection]. 1649 35

The development of hepatocellular carcinoma (HCC), the mechanisms of hepatocarcinogenesis, the prevention of HCC, and screening for HCC will be discussed. Cirrhosis has been considered as a pre-neoplastic condition for the development of HCC. The worldwide incidence of HCC differs according to different hepatitis viruses, and information is lacking. Hepatocarcinogenesis is a multistep process involving a number of different genetic alterations and is poorly understood. Interferon should help prevent the development of HCC in patients with chronic hepatitis C. Screening is the only practical approach for improving the management of HCC patients, as early detection increases the application of curative treatments. However, the cost-effectiveness of various screening strategies needs to be analysed.
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PMID:Hepatocellular carcinoma development in cirrhosis. 1722 3

Hepatoportal sclerosis (HPS) is one of the causes of noncirrhotic portal hypertension. In general, hepatic synthetic function is preserved and treatment is aimed at relief of the portal hypertension. In this study, we present the clinical and pathologic features of HPS cases who underwent liver transplantation (LT). LT cases with confirmed gross and microscopic diagnosis of HPS are included. Weight of the explanted liver, presence of thrombi in the main blood vessels, and gross and microscopic characteristics were assessed. Clinical information was gathered from chart review. From 1995 to 2004, 8 LT patients were diagnosed with HPS. Cirrhosis resulting from alcohol (2), autoimmune hepatitis (2), and hepatitis B (1), or cryptogenic cirrhosis (3) was the presumed diagnoses pre-LT. Seven patients presented with bleeding varices and 5 had concomitant ascites. At the time of LT, mean values were: prothrombin time of 15.2 seconds, serum albumin 3.2 g/dL, serum bilirubin 3.5 mg/dL, alkaline phosphatase 140 IU/L, aspartate aminotransferase 39.4 IU/L, and alanine aminotransferase 34.7 IU/L. Explanted livers were shrunken, with weights ranging from 715 to 1199 g (mean 934). Nonocclusive portal vein thrombosis was present in 2 patients. On histologic examination, there was dense portal fibrosis, marked phlebosclerosis, and presence of variable degrees of megasinusoid formation. Four livers also had features of incomplete septal cirrhosis. None showed histologic features of the presumed underlying liver disease. In conclusion, HPS can cause hepatic synthetic dysfunction that may necessitate LT. Small liver volume, significant portal fibrosis, and phlebosclerosis may contribute to hepatic parenchymal loss and subsequent synthetic compromise.
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PMID:Liver failure and need for liver transplantation in patients with advanced hepatoportal sclerosis. 1741 9

This study was undertaken to report variceal rebleeding and survival after small-diameter prosthetic H-graft portacaval shunts (HGPCS) and to compare actual to predicted survival after shunting. Since 1987 we have prospectively followed patients after undergoing HGPCS to treat bleeding varices failing/not amenable to sclerotherapy/banding. One hundred and seventy patients underwent shunting. Cirrhosis was because of alcohol in 56%, hepatitis in 12%, both in 11%, and other causes in 21%. Child class was A for 10%, B for 28%, and C for 62%. Thirty-three patients died by 6 months, 54 by 24 months, 87 by 60 months, and 112 by 10 years, generally because of liver failure. Fifty-one patients are alive at a median of 48.3 months, 76 months +/- 57.8 (mean +/- SD). Variceal rehemorrhage was documented in 3 (2%) patients. By child class, 5-year/10-year survival rates were as follows: A 66.7/33.3%, B 48.6/15.6%, and C 29.2/7.0%. Actual survival was superior to predicted survival (Model for End-Stage Liver Disease [MELD]), (p < 0.001). Variceal rehemorrhage in patients undergoing small-diameter prosthetic H-graft portacaval shunting was very uncommon. Actual survival was superior to predicted survival (MELD). Long-term survival paralleled degree of hepatic function, although long-term survival was possible even with very advanced cirrhosis. Application of HGPCS is encouraged.
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PMID:Survival and variceal rehemorrhage after shunting support small-diameter prosthetic H-graft portacaval shunt. 1745 6

Genome scanning studies suggest an important role for genes outside the major histocompatibility complex in autoimmunity. Key candidates are those genes involved in immune regulation and preservation of immune homeostasis, including the genes involved in apoptosis. Our aim was to determine the association between the Fas gene polymorphism at position -670 and susceptibility, clinical expression, and outcome in type 1 autoimmune hepatitis (AIH). An adenosine to guanine single nucleotide polymorphism in the Fas gene (TNFRSF6) promoter was assessed in 149 well-characterized Caucasoid patients and 172 matched controls. Patients and normal subjects had the similar TNFRSF6-670 allele and genotype frequencies. Serum aspartate aminotransferase (510 +/- 77 vs 283 +/- 53 U/l), gamma-globulin (3.3 +/- 0.2 vs 2.6 +/- 0.2 g/dl), and immunoglobulin G (2976 +/- 223 vs 2324 +/- 203 mg/dl) levels were higher in patients with the guanine/guanine genotype than in those with the adenosine/adenosine genotype. Cirrhosis at presentation was more common in patients with the adenosine/adenosine or adenosine/guanine genotypes than in those with the guanine/guanine genotype (29% vs 6%). Polymorphism of the Fas gene at position -670 does not influence susceptibility to AIH, but may affect the early development of cirrhosis.
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PMID:A functional Fas promoter polymorphism is associated with a severe phenotype in type 1 autoimmune hepatitis characterized by early development of cirrhosis. 1749 46

Chronic viral hepatitis remains a major problem among patients with chronic renal failure. Hepatitis B and C viruses are frequent among dialysis patients and after renal transplantation and may significantly diminish the survival of both the patient and the graft. Hepatitis B and C viral infection in these patients is often characterized by normal transaminase levels despite viremia and progressive liver lesions. Liver biopsy remains essential for assessing the extent of liver disease. Cirrhosis is a contraindication to transplantation of only a kidney, because of elevated morbidity and mortality. A combined as liver-kidney transplantation may be considered. The best treatment of hepatitis infections is preventive: vaccination against the hepatitis B virus and attentive hygiene, especially to prevent nosocomial transmission. Among patients not awaiting transplant, antiviral treatment should be reserved for patients with active or even fibrotic liver disease. For hemodialysis patients awaiting kidney transplant: Alpha interferon is ineffective and poorly tolerated by dialysis patients. Lamivudine is effective and well tolerated, but its long-term efficacy and its optimal effective dose in dialysis patients remain unknown.
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PMID:[Chronic viral hepatitis and kidney failure]. 1829 15

Liver diseases in pregnancy may be categorized into liver disorders that occur only in the setting of pregnancy and liver diseases that occur coincidentally with pregnancy. Hyperemesis gravidarum, preeclampsia/eclampsia, syndrome of hemolysis, elevated liver tests and low platelets (HELLP), acute fatty liver of pregnancy, and intrahepatic cholestasis of pregnancy are pregnancy-specific disorders that may cause elevations in liver tests and hepatic dysfunction. Chronic liver diseases, including cholestatic liver disease, autoimmune hepatitis, Wilson disease, and viral hepatitis may also be seen in pregnancy. Management of liver disease in pregnancy requires collaboration between obstetricians and gastroenterologists/hepatologists. Treatment of pregnancy-specific liver disorders usually involves delivery of the fetus and supportive care, whereas management of chronic liver disease in pregnancy is directed toward optimizing control of the liver disorder. Cirrhosis in the setting of pregnancy is less commonly observed but offers unique challenges for patients and practitioners. This article reviews the epidemiology, pathophysiology, diagnosis, and management of liver diseases seen in pregnancy.
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PMID:Liver disease in pregnancy. 1924 87

Cirrhosis due to hepatitis C virus (HCV) infection is the current leading indication for orthotopic liver transplantation (OLT) in the world. This series reports our program's experience with the treatment of HCV infection after the development of histological hepatitis. Between March 2002 and June 2008, patients with recurrent HCV were selected for treatment if the liver biopsy showed at least the F2 degree of Metavir score. HCV viral load was measured at 4, 12 and 24 weeks as well as at the end of treatment and at 6 months thereafter for patients who became HCV RNA negative (sustained virological response [SVR]). In this period, we performed 287 liver transplantations in 279 patients, including 117 (42%) who had HCV cirrhosis as the indication for OLT of whom 25 were eligible for antiviral treatment. Twelve patients completed treatment, 7 remain on treatment, and 6 were discontinued. The principal collateral effect was anemia. Only 1 patient had an episode of acute cellular rejection, which responded to adjustment of immunosuppression. Antiviral treatment in transplanted patients was feasible and did not seem to induce severe immunological effects. Adjuvant therapies to reduce cytopenias are frequently required, principally erythropoietin. The best results were observed with the pegylated interferon alfa (PEG) plus ribavirin (RBV) group: 38.9% of SVR. We recommend antiviral treatment of eligible patients with confirmed HCV recurrence using PEG plus RBV.
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PMID:Treatment for recurrent hepatitis C virus infection after liver transplantation. 1937 81

Bile duct cells and hepatocytes differentiate from the same hepatic progenitor cells. To investigate the possible association of viral hepatitis B and C with intrahepatic cholangiocarcinoma (ICC), we conducted a retrospective case-control study using univariate and multivariate logistic analyses to identify risk factors for ICC. Besides hepatic lithiasis (25.6%; P<0.001), seropositivity for hepatitis B surface antigen (37.5% of all ICC patients; odds ratio (OR) =4.985, P<0.001) and seropositivity for hepatitis C antibodies (13.1%; OR=2.709; P=0.021) are the primary independent risk factors for ICC. Cirrhosis exerted synergic effects on the development of ICC. We compared the age distributions of viral-hepatitis associated ICC to that of viral hepatitis-associated hepatocellular carcinoma (HCC). The mean age of ICC patients with viral hepatitis B (56.4+/-11.1 years) were 9 years younger than that of ICC patients with viral hepatitis C (65.6+/-9.17 years), similar to that observed in HCC. The incidence ratio of HCC : ICC : CHC (combined hepatocellular cholangiocarcinoma) in our population was 233 : 17 : 1 consistent with the theoretic ratio of hepatocyte number to cholangiocyte number in the liver. Our findings indicated that both viral hepatitis-associated ICC and HCC shared common disease process for carcinogenesis and, possibly, both arose from the hepatic progenitor cells.
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PMID:Viral hepatitis-associated intrahepatic cholangiocarcinoma shares common disease processes with hepatocellular carcinoma. 1943 94

Non-alcoholic steatohepatitis (NASH) has been associated with hepatocellular carcinoma (HCC) often arising in histologically advanced disease when steatohepatitis is not active (cryptogenic cirrhosis). Our objective was to characterize patients with HCC and active, histologically defined steatohepatitis. Among 394 patients with HCC detected by ultrasound imaging over 8 years and staged by the Barcelona Clinic Liver Cancer (BCLC) criteria, we identified 7 cases (1.7%) with HCC occurring in the setting of active biopsy-proven NASH. All were negative for other liver diseases such as hepatitis C, hepatitis B, autoimmune hepatitis, Wilson disease, and hemochromatosis. The patients (4 males and 3 females, age 63 +/- 13 years) were either overweight (4) or obese (3); 57% were diabetic and 28.5% had dyslipidemia. Cirrhosis was present in 6 of 7 patients, but 1 patient had well-differentiated HCC in the setting of NASH without cirrhosis (fibrosis stage 1) based on repeated liver biopsies, the absence of portal hypertension by clinical and radiographic evaluations and by direct surgical inspection. Among the cirrhotic patients, 71.4% were clinically staged as Child A and 14.2% as Child B. Tumor size ranged from 1.0 to 5.2 cm and 5 of 7 patients were classified as early stage; 46% of all nodules were hyper-echoic and 57% were <3 cm. HCC was well differentiated in 1/6 and moderately differentiated in 5/6. Alpha-fetoprotein was <100 ng/mL in all patients. HCC in patients with active steatohepatitis is often multifocal, may precede clinically advanced disease and occurs without diagnostic levels of alpha-fetoprotein. Importantly, HCC may occur in NASH in the absence of cirrhosis. More aggressive screening of NASH patients may be warranted.
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PMID:Does hepatocellular carcinoma in non-alcoholic steatohepatitis exist in cirrhotic and non-cirrhotic patients? 1978 50


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